Extensor tendon rupture of the finger is a very rare complication of Kienböck's disease. However, advanced Kienböck's disease can cause an attritional rupture of extensor tendons due to displaced lunate fragment. An extensor tendon of the thumb is frequently damaged in the distal radial fracture, and an extensor tendon of the fifth finger is mainly ruptured in arthritis of distal radio-ulnar joint. On the other hand, the extensor tendons of the 2, 3 and 4 fingers are usually ruptured in advanced Kienböck's disease. We report two elderly patients diagnosed with advanced Kienböck's disease after non-traumatic rupture of extensor tendon of the fingers. Since the extensor tendon rupture in Kienböck's disease present as a loss of active extension of metacarpophalangeal joint in the central fingers, these patients should undergo imaging of the wrist joints to ascertain concomitant Kienböck's disease.
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http://dx.doi.org/10.1142/S2424835520720042 | DOI Listing |
JCI Insight
January 2025
Department of Biomedical Engineering, Oregon Health and Science University, Portland, United States of America.
Spatial profiling of tissues promises to elucidate tumor-microenvironment interactions and generate prognostic and predictive biomarkers. We analyzed single-cell, spatial data from three multiplex imaging technologies: cyclic immunofluorescence (CycIF) data we generated from 102 breast cancer patients with clinical follow-up, and publicly available imaging mass cytometry and multiplex ion-beam imaging datasets. Similar single-cell phenotyping results across imaging platforms enabled combined analysis of epithelial phenotypes to delineate prognostic subtypes among estrogen-receptor positive (ER+) patients.
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Guangzhou Laboratory, Guangzhou International Bio-Island, Guangzhou, China.
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View Article and Find Full Text PDFClin Cancer Res
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University of Lyon System, Lyon, France.
The success of targeted therapies in oncogene-driven cancer is limited by adaptive or acquired treatment resistance, leading to disease progression. A recent study reports that YAP-dependent HER3 activation constitutes a therapeutic vulnerability of adaptive resistance to RET-targeted therapies in RET-altered cancers, highlighting a promising strategy to improve RET-inhibitor tumor responses.
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Division of Nephrology and Hypertension, Department of Internal Medicine, University of Kansas Medical Centre, 3901 Rainbow Blvd, MS3002, Kansas City, KS, USA.
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J Clin Invest
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Department of Biochemistry, Molecular Biology & Biophysics, University of Minnesota, Minneapolis, United States of America.
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